NOTE PRESERVED IMAGERY FOR COLOURS IN A PATIENT WITH CEREBRAL ACHROMATOPSIA Paolo Bartolomeo1, 3, Anne-Catherine Bachoud-Lévi2, 3 and Gianfranco Denes4 (1 INSERM Unité 324, Paris, France; 2 LSCP, EHESS, CNRS, Paris, France; 3 Service de Neurologie, Hôpital Henri-Mondor, Créteil, France; 4 Dipartimento di Scienze Neurologiche e Psichiatriche, Università di Padova, Italy)

ABSTRACT We report the case of a patient who, after sequential bilateral strokes in the occipital regions sparing the primary visual cortex, developed a severe deficit of colour perception. At variance with other reports of acquired achromatopsic patients, she showed a perfectly vivid visual imagery for colours. These findings, together with similar data in domains other than colour processing, challenge the theories which posit that the same cognitive processes are involved in both the perception and the retrieval from memory of a given stimulus.

INTRODUCTION Cerebral achromatopsia is an uncommon disorder of colour perception resulting from lesions in the anterior inferior part of the occipital lobe (Meadows, 1974). Patients typically complain that they cannot see colours anymore, and the world appears uniformly grey or brown. In the case of unilateral lesion achromatopsia is confined to the contralateral visual hemifield (see Zeki, 1990, for review). According to some authors (Farah, 1988; Damasio, 1989), this perceptual deficit is always associated with an inability to recall the colour of common objects from memory (e.g., a tangerine, a poppy), a task which is often solved by imagining the relevant object in colour. Farah (1988) reviewed several case studies of acquired achromatopsic patients. She found a consistent association between impaired colour vision and impaired colour imagery, and concluded that the same neural representations are involved in seeing colours and imagining them. Additional evidence of the association between perception and imagery deficits in colour processing was provided by Damasio, Yamada, Damasio et al. (1980, case 2), Gomori and Hawryluk (1984), Levine, Warach and Farah (1985, patient 1), Rizzo, Smith, Pokorny et al. (1993), Goldenberg (1992), and Shelton, Bowers, Duara et al. (1994). These findings obtained in single-case studies are corroborated by the results of De Renzi and Spinnler (1967), who found a consistent association between “colour amnesia” (i.e., the inability to retrieve from memory the colour of an object) and perceptual colour processing deficits in an unselected group of unilaterally brain-damaged patients. The authors concluded that a deficit of colour revisualization was almost always present in patients with impaired colour perception. However, this association of deficits is far from being the rule. Patients have been described with impaired mental colour imagery and preserved colour perception, thus suggesting a possible image generation deficit (see Goldenberg, 1993, for review). Possible instances of the opposite dissociation, namely colour perceptual deficit with intact colour imagery, have also been reported. The patient described by Meadows (1974, appendix; Pearlman, Birch and Meadows, 1979) was able to name the colours of common objects either spoken by the examiner or presented as black and white images. Also other Cortex, (1997) 33, 369-378

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achromatopsic patients had no difficulty in naming the colours of common objects from memory (Green and Lessell, 1977; Heywood, Wilson and Cowey, 1987; Scarpatetti, Ketz and Jung, 1983). It must be noted, however, that in these studies the results of colour imagery tests are only cursorily reported, and all details on the questions are not given. This is a crucial point, since these patients’ good performance could rely on a verbal association strategy rather than on the inspection of centrally generated images. Indeed, the colour of the items provided as examples by Meadows (grass, banana, fire-engine, London bus) may be recalled using verbal semantic knowledge. That achromatopsic patients can use a verbal strategy to answer colour-from-memory questions is strongly suggested by the report of a Belgian achromatopsic patient of Italian origin (Dumont, Griggio, Dupont et al., 1981). She enumerated in Italian the colours of the Italian flag, but was not able to say the colours of the Belgian flag, although she had been living in Belgium for decades. A more direct demonstration of the use of different strategies in these tasks was provided by Beauvois and Saillant (1985), whose patient R.V. was better in retrieving colour names using verbal strategies than using visual imagery, even when the same colour was concerned (e.g., R.V. was better on question like “what do people say when asked what colour snow is?” than answering questions like “imagine a beautiful snowy landscape... Can you see it? Well, now tell me what colour the snow is”). A similar dissociation was described by De Vreese (1991, case II). Unequivocal evidence of a dissociation between perceptual colour processing and colour imagery abilities is provided by the present case study1. CASE REPORT Madame D is a 74-year-old right-handed housewife who had worked as a secretary and loved painting in oils as a hobby. She suffered in May 1995 from a haematoma located across the left temporo-occipital sulcus, involving the middle occipital gyrus and the inferior temporal gyrus (Brodmann areas 18, 19 and 37). She presented with a right homonymous

A

B Fig. 1 – T1 weighted MRI showing a left-sided lesion tying across the temporo-occipital sulcus and a right-sided lesion centred on the middle occipital gyrus.

1 Since submission of this paper, an achromatopsic patient has been described (Shuren, Brott, Schefft et al., 1996) with an unquestionable preservation of mental imagery for colours.

Colour imagery in cerebral achromatopsia

Fig. 2 – Goldmann perimetry showing a central scotoma with II/4 testing.

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Fig. 3 – Mme D’s performance on the Farnsworth (1947) dichotomous test. Normal subjects’ diagram follows the contours. Colour-blind subjects’ performance is characterised by two or more lines crossing the diagram. The lack of any definite confusion axes is a frequent feature in cerebral, as opposed to congenital, achromatopsia (see, e.g., McCarthy and Warrington, 1990; Meadows, 1974).

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hemianopia and showed a mild anomia, without any comprehension or repetition deficit, that subsided after some weeks. No other linguistic deficits were present, apart from a pure alexia (which will be the focus of a subsequent article). After some weeks, her visual field defect had resolved on confrontation testing. Goldmann perimetry showed a residual right paracentral scotoma, which disappeared with IV/4 test. She named correctly and without hesitation 20 colours (see below, Colour Naming, for description of the test material). Colour identification in the right visual hemifield was also flawless on clinical testing: The colour of 4 × 4 cm colour patches presented at about 30° to the right of fixation on the horizontal midline was identified rapidly and without errors. At that time, Mme D’s only complain was her reading difficulty. Since she could not enjoy reading anymore, Mme D occupied herself almost exclusively by painting. At that time, she never complained about problems with colours or colour mixtures. In December 1995 she suffered from a second, right-sided haematoma, almost symmetrical to the first. The lesion was centred to the middle occipital gyrus, just posteriorly to the temporo-occipital sulcus. It involved area 19 and the white matter underlying area 18 (Figure 1). After the occurrence of the second stroke, Mme D found herself unable to recognise familiar faces and common objects by sight, and complained of seeing the world in shades of grey. She had full visual field on confrontation testing. Goldmann perimetry showed a central scotoma with II/4 test (Figure 2). Visual evoked responses with black and white pattern were normal for latency and amplitude. Mme D obtained a verbal IQ of 109 on the WAIS-R. She performed at chance level on a modified version of the Efron test (Warrington and James, 1988) and on the shape detection screening test of the Visual Object and Space Perception Battery (Warrington and James, 1991). She was unable to name any black-andwhite realistic drawings. When asked to name real objects presented by the examiner, she was 13/35 correct on visual presentation, claiming that she was unable to recognise the other items. Examples of wrong responses in this task include ring → “coin”, telephone → “wall diary”, glass → “alarm clock”. She correctly named the same objects when they produced some noise (e.g., jiggling keys) or on tactile presentation. Formal colour testing began on February, 1996. By that time, Mme D claimed that her visual world had changed from grey to a reddish-brownish appearance, and reported to have occasionally perceived bright, saturated colours (e.g., she correctly identified the red of a truck moving on the road). PERCEPTUAL COLOUR TESTING Colour Discrimination The Farnsworth D-15 test (Farnsworth, 1947) was administered on two different occasions. The patient’s performance was grossly defective (Figure 3). Mme D was well aware of her difficulties, and looked at each patch for a long time before arranging it. She never attempted to name the colours of the patches. Mme D correctly identified the first and last items of the Ishihara (1974) plates, as colourblind subjects can do. She was permitted to follow the targets’ contour of the other items with her index finger, on account of her alexia. She found the task difficult, and outlined correctly 7 targets (items 2, 3, 9, 15, 16, 17). This result indicates a pathological performance. Colour Matching The patient was presented with a 16 × 20 cm board composed of 20 4 × 4 cm different colour patches and 20 separate 4 × 4 cm colour patches that she had to match with the corresponding colours on the board. Again she looked puzzled and performed the test slowly and hesitantly. She was 6/20 correct, when matching the orange, white, sky blue, dark green, royal blue and light brown patches. Colour Pointing Mme D was asked to point to the colours spoken by the examiner. The same plate was used as in the preceding test. The patient was 8/20 correct, when pointing to the green, black, orange, chestnut brown, white, dark green, royal blue and pink patches.

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Colour Naming Mme D was shown the same colour board and asked to name the colour pointed by the examiner. The test was administered twice on different days. As with the previously described tests, she was slow and hesitant in responding, carefully examining the patches and often expressing doubts about her responses. Occasionally, she remarked that colours changed in hue before her eyes. The overall correct performance was 8/40. In half of the cases the patient perseverated on some colour names (beige nine times, green seven times, yellow and brown four times). Names of the colour stimuli and patient’s responses on the two test sessions are reported in the Appendix. Mme D showed the same degree of impairment on naming, matching and pointing to colours (x2 = 2.76, d.f. = 2, p n.s.). A qualitative comparison among the results of colour perceptual tests does not seem to suggest any consistent patterns of impairment on particular colours. For example, while green appeared to be relatively spared in some tests (it was correctly pointed at, it was named two times out of four, and it was present in all the identified items of the Ishihara plates), green patches were also erroneously arranged next to ochre, blue and violet in the Farnsworth test. Colour Imagery Tasks Colour Verbal Memory Mme D was asked to say the appropriate colour of 20 objects indicated verbally by the examiner (De Renzi and Spinnler, 1967). She named quickly and correctly all the 20 colours, sometimes employing expressions that suggested the use of visual imagery rather than a verbal association strategy (e.g., wheat → “cream-coloured, pale yellow”). Equally flawless was the patient’s performance on 15 items of the “verbo-visuo-verbal test” devised by Beauvois and Saillant (1985, appendix 3, experiment 2). Analysis of Mme D’s responses suggested that she again relied on a mental imagery strategy (e.g., interior part of a radish → “white, with pale red streaks”; champagne wine → “it can be either pink or golden”; pastis → “opaline”). Colour-object Fluency (De Vreese, 1988) The patient was asked to produce the name of as many objects as possible which are typically red, green, yellow and black. A time limit of 60 sec was allowed for each colour. Her score, 23 according to De Vreese’s procedure, was largely higher than normative data (controls’ mean score: 14.07 ± 3.98). Colouyr Name Fluency (De Vreese, 1991) Although this test does not necessarily require imagery abilities, it was administered to our patient in order to confirm the integrity of her colour lexicon. Mme D was asked to produce as many colour names as possible in 60 sec. She produced 14 colour names (controls’ mean score: 10.41 ± 2.15). Mental Hue Comparison A modified version of a test devised by De Vreese (1991) was developed. Twenty-five pairs of items were proposed verbally by the examiner. Each pair was composed of objects of the same colour with a different hue (e.g., French bean/bay leaf, interior of a pineapple/ interior of a potato, cherries/strawberries, Paris metro ticket/pine). The patient was asked to say which of the items within a pair was darker in colour. Mme D was 24/25 correct. The only response that was considered as wrong was “potatoes are darker than chestnuts”. On subsequent questioning, the patient explained that chestnuts are shiny, while potatoes are brown with a dull grey appearance.

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DISCUSSION Here we have reported the case of a patient who developed full-field achromatopsia following sequential bilateral occipital lesions. In fact, the symptom was not present following the first, left-sided occipito-temporal lesion, but it appeared when a second, symmetrical lesion in the right occipital cortex occurred. This puzzling sequence of events is difficult to reconcile both with the well known case descriptions of hemiachromatopsia due to unilateral lesion and with PET studies reporting a response to colour stimuli larger on the left than on the right side (Corbetta, Miezin, Dobmeyer et al., 1990; Lueck, Zeki, Friston et al., 1989; Zeki, Watson, Lueck et al., 1990). A subclinical hemi- or free field achromatopsia after the first left-sided occipital lesion cannot be excluded, but it would be surprising, given the pleasure that Mme D found in painting at that tirne. More in general, our data could support the notion of a critical role of the right hemisphere in colour processing (see, e.g., De Renzi and Spinnler, 1967; Davidoff, 1991). Our patient’s pattern of performance is relevant as concerns the relationship between perceptual and imagery processes. Visual imagery deficits often parallel visual perceptual deficits in the same domain. This observation led some authors (Damasio, 1989; Farah, 1988, 1989; Kosslyn, 1994) to postulate a common neural substrate for perception and imagery, i.e., specialised, domain-specific cortical areas would be used to process the same kind of information (e.g., colours) in perception and retrieval from memory. However, perceptual and imagery deficits can dissociate one from another in several domains. Visual imagery can be spared in cases of cortical blindness (Chatterjee and Southwood, 1995; Goldenberg, Mullbacher and Nowak, 1995) and object agnosia (Behrmann, Moscovitch and Winocur, 1994; Servos and Goodale, 1995), and Behrmann et al.’s metanalysis of previous reports makes the case for a double dissociation between perceptual and imagery deficits of objects. Perri, Bartolomeo and Silveri (1996) described a pure alexic patient who showed a perceptual deficit of letter identification in the absence of any deficit of visual imagery for letters. Also prosopagnosic patients can be able to imagine faces (Hécaen, Ajuriaguerra, Magis et al., 1952). Moreover, dissociations between performance on visual and imagery tasks can be observed in patients with unilateral spatial neglect (Anderson, 1993). In a group study, Bartolomeo, D’Erme and Gainotti (1994) found that only a minority of visual neglect patients showed signs of neglect on description from memory of familiar places (a task devised by Bisiach and Luzzatti, 1978). Moreover, the possibility exists of an imaginal neglect in the absence of, or after recovery from, visuospatial neglect (Bartolomeo et al., 1994; D’Erm, Bartolomeo and Gainotti, 1994; Guariglia, Padovani, Pantano et al., 1993). In Kosslyn’s (1994) and Farah’s (1984) models, colour perception and colour imagery share a common visual buffer, in which both mental and physical colour percepts occur. Through a generation process, the content of long-term memory is transferred onto the visual buffer, where it can be inspected for further processing. According to this model, a selective deficit of the generation process should result in impaired imagery coupled with intact perception (recognition would be possible through a direct access to long-term memory representations) (Farah, 1984). The opposite dissociation, namely impaired perception and intact imagery, should occur following a deficit of perceptual access to intact visual representations. In Kosslyn’s words, “problems in perceptual organization or in matching input to stored visual representations in the pattern activation subsystems can impair perception but leave imagery relatively intact (1994, p. 329)”. In our patient, however, visual imagery for colours was not only “relatively” spared, but perfectly vivid, despite a striking impairment of colour perception. The hypothesis of a problem of matching between visual input and stored visual representations does not fit with the clinical reality of Mme D’s perception of the world as drained of colours, and her inability not only to identify but also to discriminate between colours. According to Kosslyn (1994), the visual buffer is a structure in the occipital lobe, composed of retinotopically organised areas from V1 to V4. An impairment of early sensory analysis (i.e., from the retina to V1) can be reasonably ruled out in our patient, given the lack of clinical, neuroradiological and neurophysiological evidence of damage to the visual system prior to the extrastriate areas (apart from the small visual field deficit, which obviously cannot account

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for the achromatopsia). Assuming Kosslyn’s model, the functional locus of impairment in our patient should be at the level of the visual buffer, challenging the claim (Farah, 1984; Kosslyn, 1994) that a single visual buffer constitutes the common “screen” for perceptual and imagery processes. From the anatomo-functional point of view, our patient’s pattern of spared colour memories in the absence of colour perception does not easily accommodate with Damasio’s (1989) hypothesis that memory contents are retrieved through the retroactivation of the very same cortical areas that had processed the revelant information during perception. These “early cortices” include the primary and first-order associative sensory cortices. According to Damasio, “no other cortices, and certainly no other higher order, integrative cortices, are capable of supporting the recall of the perceptually impaired feature (1989, p. 33)”. Our patient’s achromatopsia can be explained either by direct damage to a cortical area specialised for colour processing (possibly the human homologue of V4, located in the prestriate cortex [Corbetta, Miezin, Dobmeyer et al., 1990; Zeki, Watson, Lueck et al., 1990]), or by a disconnection of V4 from the primary visual areas (V 1). In the first case, Damasio’s hypothesis is directly disconfirmed. As for the hypothesis of a disconnection between intact V4 and V1 areas, it explains Mme D’s pattern of impairment. But even in this case a difficulty arises with Damasio’s hypothesis. According to Damasio, Mme D’s vivid visual memories should depend on the retroactivation of V1, but this would be an implausible mechanism if this area were disconnected from more anterior areas, such as V4. Our case can be explained in a much easier way by postulating different cortical implementations of perceptual and imagery colour processing. In a PET experiment (Martin, Haxby, Lalonde et al., 1995), subjects had to generate the name of colours associated with an achromatic line drawing of an object, or with its written name. In both conditions, a region was activated in the ventral temporal lobe, 2 to 3 cm anterior to the region of the fusiform gyrus activated by colour perception (Corbetta et al., 1990; Zeki et al., 1993). Provided that subjects used a colour-imagery strategy to perform the task, the data would suggest that distinct cortical regions are implied in perceptual analysis and imagery of colours. The fact that these cortical areas lie close to one another would make them liable to be damaged at the same time, thus accounting for the frequent observation of an association between perceptual and imagery deficits in colour processing. Additional support for this interpretation of our patient’s pattern of performance comes from the report (Luzzatti and Davidoff, 1994) of two patients with the opposite dissociation to the one showed by Mme D. These two patients had preserved colour perception and impaired retrieval of knowledge concerning the colours of objects. Interestingly, their lesions, caused by herpes simplex encephalitis, appeared to affect regions anterior to the location of Mme D’s lesions. The possibility that perception and imagery are implemented in distinct cortical areas is a disappointing one for those of us who followed with interest the attempts to establish a neural equivalence between the two processes. Nevertheless, this possibility is reassuring in that it seems to confirm common experience: That seeing something for real is quite different from imagining it – unless, of course, one suffers from hallucinations. Acknowledgements. This work was supported by the European Union grant n. ERBCHBGCT930344 to P.B. and by an INSERM grant to G.D. We are grateful to Madame D and her husband for their good humour and friendly attitude, and to J.-D. Degos for permission to study the patient and for helpful discussion. Thanks are also due to M. Magne and M.-F. Boissé for standard neuropsychological testing, to P. Brugières for evaluation of MRI data, and to A. Petrov for reviewing the English.

REFERENCES ANDERSON, B. Spared awareness for the left side of internal visual images in patients with left-sided extrapersonal neglect. Neurology, 43: 213-216, 1993. BARTOLOMEO , P., D’ERME, P., and GAINOTTI G. The relationship between visuospatial and representational neglect. Neurology, 44: 1710-1714, 1994.

Colour imagery in cerebral achromatopsia

377

BEAUVOIS, M.F., and SAILLANT, B. Optic aphasia for colours and colour agnosia: A distinction between visual and visuo-verbal impairments in the processing of colours. Cognitive Neuropsychology, 2: 1-48, 1985. BEHRMANN, M., MOSCOVITCH, M., and WINOCUR, G. Intact visual imagery and impaired visual perception in a patient with visual agnosia. Journal of Experimental Psychology: Human Perception and Performance, 20: 1068-1087, 1994. BISIACH, E., and LUZZATTI, C. Unilateral neglect of representational space. Cortex, 14: 129-133, 1978. CHATTERJEE, A., and SOUTHWOOD, M.H. Cortical blindness and visual imagery. Neurology, 45: 21892195, 1995. CORBETTA, M., MIEZIN, F.M., DOBMEYER, S., SHULMAN, G.L., and PETERSEN, S.E. Attentional modulation of neural processing of shape, color, and velocity in humans. Science, 248: 1556-1559, 1990. D’ERME, P. BARTOLOMEO, P., and GAINOTTI, G. Difference in recovering rate between visuospatial and representational neglect. Paper presented at the International Neuropsychological Society, 17th Annual European Conference, Angers, France, 1994. DAMASIO, A. Time-locked multiregional retroactivation: A system-level proposal for the neuronal substrates of recall and recognition. Cognition, 33: 25-62, 1989. DAMASIO, A., YAMADA, T., DAMASIO, H., CORBETT, J., and MCKEE, J. Central achromatopsia: Behavioral anatomic, and physiologic aspects. Neurology, 30: 1063-1071, 1980. DAVIDOFF, J. Cognition through Color. Cambridge, Mass.: The MIT Press, 1991. DE RENZI, E., and SPINNLER, H. Impaired performance on color tasks in patients with hemispheric damage. Cortex, 3: 194-217, 1967. DE VREESE, L.P. Category-specific versus modality-specific aphasia for colours: A review of the pioneer case studies. International Journal of Neurosciences, 43: 195-206, 1988. DE VREESE, L.P. Two systems for colour-naming defects: Verbal disconnection vs colour imagery disorder. Neuropsychologia, 29: 1-18, 1991. DUMONT, J., GRIGGIO, A., DUPONT, H., and JACQUY, J. A propos d’un cas d’agnosie visuelle avec prosopoagnosie et agnosie des couleurs. Acta Psychiatrica Belgica, 81: 25-45, 1981. FARAH, M. The neurological basis of mental imagery: A componential analysis. Cognition, 18: 245272, 1984. FARAH, M. Is visual imagery really visual? Overlooked evidence from neuropsychology. Psychological Review, 95: 307-317, 1988. FARAH, M. The neural basis of mental imagery. Trends in Neurosciences, 12: 395-399, 1989. FARNSWORTH, D. Farnsworth Dichotomous Test for Colour-blindness – Panel D-15. New York: The Psychological Corporation, 1947. GOLDENBERG, G. Loss of visual imagery and loss of visual knowledge – A case study. Neuropsychologia, 30: 1081-1099, 1992. GOLDENBERG, G. The neural basis of mental imagery. Baillière’s Clinical Neurology, 2: 265-286, 1993. GOLDENBERG, G., MULLBACHER, W., and NOWAK, A. Imagery without perception – A case study of anosognosia for cortical blindness. Neuropsychologia, 33: 1373-1382, 1995. GOMORI, A.J., and HAWRYLUK, G.A. Visual agnosia without alexia. Neurology, 34: 947-950, 1984. GREEN, G.J., and LESSELL, S. Acquired cerebral dyschromatopsia. Archives of Ophtalmology, 95: 121128, 1977. GUARIGLIA, C., PADOVANI, A., PANTANO, P., and PIZZAMIGLIO, L. Unilateral neglect restricted to visual imagery. Nature, 364: 235-237, 1993. HÉCAEN, H., AJURIAGUERRA , J., MAGIS, C., and ANGELERGUES , R. Le problème de l’agnosie des physionomies. L’Encéphale, 41: 322-355, 1952. HEYWOOD, C.A., WILSON, B., and COWEY, A. A case study of cortical colour “blindness” with relatively intact achromatic discrimination. Journal of Neurology, Neurosurgery and Psychiatry, 50: 22-29, 1987. ISHIHARA, S. Tests for Colour-blindness. Tokyo: Kanehara Shup, 1974. KOSSLYN, S.M. Image and Brain: The Resolution of the Imagery Debate. Cambridge, Mass: The MIT Press, 1994. LEVINE, D.N., WARACH, J., and FARAH, M. Two visual systems in mental imagery: Dissociation of “what” and “where” in imagery disorders due to bilateral posterior cerebral lesions. Neurology, 35: 1010-1018, 1985. LUECK, C.J., ZEKI, S., FRISTON, K.J., DEIBER, M.P., COPE, P., CUNNINGHAM , V.J., LAMMERTSMA, A.A., KENNARD, C., and FRACKOWIAK, R.S.J. The colour centre in the cerebral cortex of man. Nature, 340: 386-389, 1989. LUZZATTI, C., and DAVIDOFF, J. Impaired retrieval of object-colour knowledge with preserved colour naming. Neuropsychologia, 32: 933-950, 1994. MARTIN, A., HAXBY, J.V., LALONDE, F.M., WIGGS, C.L., and UNGERLEIDER, L.G. Discrete cortical regions associated with knowledge of color and knowledge of action. Science, 270: 102-105, 1995. MCCARTHY, R.A., and WARRINGTON, E.K. Cognitive Neuropsychology: A Clinical Introduction. San Diego: Academic Press, 1990.

378

P. Bartolomeo and Others

MEADOWS, J.C. Disturbed perception of colours associated with localized cerebral lesions. Brain, 97: 615-632, 1974. PEARLMAN, A.L., BIRCH, J., and MEADOWS, J.C. Cerebral color blindess: An acquired defect in hue discrimination. Annals of Neurology, 5: 253-261, 1979. PERRI, R., BARTOLOMEO, P., and SILVERI, M.C. Letter dyslexia in a letter-by-letter reader. Brain and Language, 53: 390-407, 1996. RIZZO, M., SMITH, V., POKORNY, J., and DAMASIO, A. Color perception profiles in central achromatopsia. Neurology, 43: 995-1001, 1993. SCARPATETTI, A., KETZ, E., and JUNG, W. Zentral bedingte Achromatopsia. Klinische Monätsblatter für Augenheilkunde, 183: 132-135, 1983. SERVOS, P., and GOODALE, M.A. Preserved visual imagery in visual form agnosia. Neuropsychologia, 33: 1383-1394, 1995. SHELTON, P.A., BOWERS, D., DUARA, R., and HEILMAN, K.M. Apperceptive visual agnosia. A case study. Brain and Cognition, 25: 1-23, 1994. SHUREN, J.E., BROTT, T.G., SCHEFFT, B.K., and HOUSTON, W. Preserved color imagery in an achromatopsic. Neuropsychologia, 34: 485-489, 1996. WARRINGTON, E.K., and JAMES, M. Visual apperceptive agnosia: A clinico-anatomical study of three cases. Corxex, 24: 13-32, 1988. WARRINGTON, E.K., and JAMES, M. The Visual Obiect and Space Perception Battery. Bury St. Edmunds: Thames Valley Test Company, 1991. ZEKI, S. A century of cerebral achromatopsia. Brain, 113: 1721-1777, 1990. ZEKI, S. A Vision of the Brain. Oxford: Blackwell Scientific Publications, 1993. ZEKI, S., WATSON, J.D.G., LUECK, C.J., FRISTON, K.J., KENNARD, C., and FRACKOWIAK , R.S.J. A direct demonstration of functional specialization in human visual cortex. The Journal of Neuroscience, 11: 641-649, 1990. Paolo Bartolomeo, INSERM Unité 324, Centre Paul Broca, 2ter rue d’Alésia, 75014 Paris, France. E-mail: [email protected]. fr.

(Received 28 April 1996; accepted 13 July 1996)

APPENDIX Responses Produced by Mme D on the Colour Naming Test Stimulus

1st session

2nd session

Green Red Black Orange Mauve Chestnut brown Pale yellow Violet Ochre White Crimson Yellow Golden yellow Pastel green Sky blue Dark green Royal blue Dark grey Light brown Pink

Beige Pink, not red Grey or brown Light beige Dark beige Green Beige Light brown Dark yellow Light yellow No answer Yellow (+), beige Beige Blue Blue-green Green (+) Green Green Beige (+) Beige

+ + Brown Red Brown Grey Pink Red Brown Pink Dark red (+) Yellow, grey, yellow (+) Ochre Blue Green Grey + Grey-beige Orange Green